Until recently, the treatment of cancer has been largely focused on the development of therapeutic agents or techniques that kill cancer cells. For example, most chemotherapeutic drugs work by impairing mitosis (cell division), effectively targeting fast-dividing cells. As these drugs cause damage to cells they are termed cytotoxic. Some drugs work by causing cells to undergo apoptosis (so-called “cell suicide”). Unfortunately, scientists have yet to be able to locate specific features of malignant and immune cells that would make them uniquely targetable (barring some recent examples, such as the Philadelphia chromosome as targeted by imatinib). This means that other fast dividing cells such as those responsible for hair growth and for replacement of the intestinal epithelium (lining) are also affected.
Because chemotherapy affects cell division, both normal and cancerous cells are susceptible to the cytotoxic effects of chemotherapeutic agents. Success of conventional chemotherapeutic regiment is based on the principle that tumors with high growth fractions (such as acute myelogenous leukemia and the lymphomas, including Hodgkin's disease) are more sensitive to chemotherapy because a larger proportion of the targeted cells are undergoing cell division at any given time. This strategy often results in undesirable side-effects such as hair loss and normal tissue/organ damage. It also has severe limitations on the dosage of chemotherapeutic agents that can be administered to a patient, thus, limiting the effective range of chemotherapy.